Essential hypertension is a major cause of cardiovascular disease. Its etiologies are thought to involve both genetic and environmental factors. Elevated blood lead levels have been indicated as contributing factor in essential hypertension. It is unclear how lead exerts this effect. The purpose of this investigation is to consider endothelial nitric oxide synthase (eNOS) inhibition as a mechanism for this effect, using a population based approach and a recently reported Glu298Asp substitution polymorphism in eNOS. Specific Aims: 1) Describe the relation of the eNOS Glu298Asp polymorphism and blood pressure in this cohort. 2) Describe how the relation of lead and blood pressure varies by the eNOS Glu298Asp polymorphism in this cohort. Methods: This will be a cross-sectional study of lead exposed workers and unexposed controls. Blood pressure and lead levels in these workers have been recorded, and blood samples have been taken. The blood samples will be genotyped for the Glu298Asp polymorphism. Linear regression models will be developed to examine the relation of lead and blood pressure in these workers. We will also consider stratified analyses, looking at odds ratios of hypertension. If eNOS is involved in lead induced increases in blood pressure, the lead-blood pressure relationship (the regression slopes or the odds ratios for hypertension) should different for individuals with and without Asp-variant eNOS.